This research seeks to discover the relationships between superoxide (O2), superoxide disumtase (SOD), long-wave ultra-violet light (UV), hyperoxia and certain types of cataracts. It is hypothesized that the effect of oxygen or UV on the lens is mediated by the formation of superoxide (also possibly hydrogen peroxide (H2O2) and the hydroxyl free radical (OH) ) and this effect is modified by the relative activity of the dismutase. A clear connection will be sought between UV and O2 generation. The chief analytical procedure will be a kinetic enzymatic assay for SOD. This reaction will also serve as a probe for O2 and, in conjuction with specific metabolic inhibitors and free radical scavengers, will yield information concerning the involvement of O2 and the other toxic oxygen free radicals in producing cataractous changes resembling human senile cataracts. The animals to be used are rat, mouse, chick, and pigeon; other species will be considered. Also under investigation are the lenses of mice from a colony which is yielding a reasonable number of late-appearing cataracts. We propose this as a model for human senile cataract.